Unpremedicated Dogs Research Articles

Effects of propofol alone or in combination with ketamine on intraocular pressure in unpremedicated dogs.

To determine the effects of propofol (P) alone and in combination with ketamine (KP) at ratios of 1:1, 1:2, and 1:3 on intraocular pressure (IOP) in unpremedicated dogs. A total of 28 cross-bred healthy dogs. Dogs were randomly assigned to one of four groups (n = 7 per group) to receive intravenous P or KP at 1:1, 1:2, and 1:3 ratios, respectively. The infusion was administered at 0.6 mg/kg/min for 60 min. IOP, cardiorespiratory variables, rectal temperature (RT), and pedal reflex were recorded every 5 min for 60 min, starting from baseline (BL). There was a statistically significant increase in IOP in all groups: P (p = .011), KP 1:1 (p = .003), KP 1:2 (p = .023), and KP 1:3 (p = .008). The IOP increase was less pronounced in the KP 1:2 group and was only significant (p = .023) at T45 compared with BL. A significant correlation was observed between IOP and SpO2 in P (r = -.215, p = .02), KP 1:2 (r = -.579, p < .01), and KP 1:3 (r = -.402, p < .01) groups. IOP significantly increased due to decreased SpO2 below 86.5% (p < .05). Propofol alone and in combination with ketamine may increase preexisting IOP in unpremedicated dogs. SpO2 levels below 86.5% may trigger an increase in IOP. Administering KP in a 1:2 ratio at an infusion rate of 0.6 mg/kg/min does not significantly alter IOP for under 45 min in unpremedicated dogs with sufficient oxygenation.

Cardiorespiratory and anesthetic effects of clinical and supraclinical doses of alfaxalone in dogs

ObjectiveTo determine the cardiorespiratory and anesthetic effects of 2, 6, and 20 mg kg−1 IV alfaxalone in hydroxypropyl beta cyclodextrin (Alfaxan) in dogs. Study designBlinded four-way crossover randomized by dose. AnimalsEight healthy adult purpose-bred mixed breed dogs (four male, four female) weighing between 12 and 28 kg. MethodsFour (0, 2, 6, 20 mg kg−1) IV treatments of alfaxalone were administered to each dog with a 3-hour washout period between doses. Measurements of heart rate, aortic systolic, mean, and diastolic blood pressures, pulmonary arterial and right atrial mean pressures, cardiac output, respiratory rate, tidal and minute volumes, and arterial blood pH, blood gases (PaO2, PaCO2) were performed prior to and at predetermined intervals after drug administration. Systemic vascular resistance and rate pressure product were calculated. The quality of induction, maintenance, and recovery from anesthesia were categorically scored as was the response to noxious stimulation. ResultsThe administration of alfaxalone resulted in dose-dependent changes in cardiovascular and respiratory parameters. Decreases in arterial blood pressure and increases in heart rate occurred at higher doses with most variables returning to baseline in 15–30 minutes. Respiratory rate, minute volume, and PaO2 decreased and apnea was the most common side effect. The duration of anesthesia increased with dose, and induction, maintenance, and recovery were judged to be good to excellent with all doses studied. Conclusions and clinical relevanceAlfaxalone produced good to excellent short-term anesthesia in unpremedicated dogs. Cardiorespiratory effects were minimal at lower doses. Anesthesia was judged to be good to excellent and associated with unresponsiveness to noxious stimulation for the majority of anesthesia. Hypoventilation and apnea were the most prominent and dose-dependent effects.

Effects of isoflurane on echocardiographic parameters in healthy dogs

ObjectiveTo study the echocardiographic effects of isoflurane at an end-tidal concentration approximating 1.0 times the minimum alveolar concentration (MAC) in healthy unpremedicated dogs. Study designProspective experimental trial. AnimalsSixteen mature mongrel dogs of either sex weighing 11.06 ± 2.72 kg. MethodsAfter performing a baseline echocardiogram in the awake animal, anesthesia was induced with increasing inspired concentrations of isoflurane via a face mask until tracheal intubation was possible. Following intubation, the end-tidal concentration was decreased to 1.4% for the rest of the anesthetic period. Serial echocardiograms were recorded at 25, 40, and 55 minutes after the end-tidal concentration was reached. ResultsNo changes were observed in heart rate. However, significant decreases were seen in left ventricular end-diastolic diameter (Mean maximal change: 13.8%), interventricular septal thickness during systole (15.2%), interventricular septal thickening fraction (72.2%), left ventricular free wall thickening fraction (63.5%), ejection fraction (39.9%), and fractional shortening (46.7%). In addition, peak flow velocities across mitral, pulmonic, and aortic valves were significantly lower than baseline values. Decreases were also observed in end-diastolic left ventricular volume index (approximately 32.1% from the awake value), stroke index (58.2%), and cardiac index (55.3%) when compared with awake measurements. Conclusions and clinical relevanceOur results indicate that 1 × MAC isoflurane caused significant myocardial depression in healthy dogs. These changes in myocardial function need to be considered carefully when isoflurane is to be used in dogs with poor cardiovascular reserve.

Effects of diazepam, ketamine, and their combination on intraocular pressure in normal dogs

Ketamine has been implicated as causing increases in intraocular pressure. The purpose of this study is to document the effects of ketamine, diazepam, and their combination on intraocular pressure (IOP) in normal, unpremedicated dogs. Random-source dogs were assigned to one of five groups of 10 dogs each: ketamine 5 mg kg–1 (KET5), ketamine 10 mg kg–1 (KET10), diazepam 0.5 mg kg–1 (VAL), ketamine 10 mg kg–1 with diazepam 0.5 mg kg–1 (KETVAL), saline 0.1 mL kg–1 (SAL), all given intravenously. A baseline IOP was measured before injection, immediately after injection, and at 5, 10, 15, and 20 minutes following injection. IOP was increased over baseline immediately after injection in the KET5, KET10, and KETVAL groups; at 5, 10, and 15 minutes in the KET5 group; and at 20 minutes in the KETVAL group. The mean IOP change compared to SAL increased immediately after injection and at 5 minutes in the KET5, KET10, and KETVAL groups; at 10 and 15 minutes in the KET5 group, and at 20 minutes in the KETVAL group. The mean IOP increased up to 5.7, 3.2, and 3.1 mm Hg over mean baseline in the KET5, KET10, and KETVAL groups, respectively. All dogs in the KET5 group and the majority in the KETVAL and KET10 groups had an increase in their IOP over baseline. Ketamine caused a clinically and statistically significant elevation in IOP over baseline and compared to SAL. The concurrent addition of diazepam did not blunt this increase. Ketamine should be avoided in dogs with corneal trauma, glaucoma, or in those undergoing intraocular surgery.

Comparison of sevoflurane and isoflurane anesthetic index in unpremedicated dogs

Anesthetic respiratory effects of sevoflurane (SEVO) were compared with isoflurane (ISO) in unpremedicated dogs. Minimum alveolar concentration (MAC), apneic concentration (AC), and anesthetic index (AI) of SEVO and ISO were determined in eight 1-year-old healthy dogs, weighing 19 ± 3 kg (mean ± SEM) in a randomized complete block multiple cross-over design. Dogs were mask-induced with either SEVO or ISO in 100% oxygen. Following endotracheal intubation, dogs were instrumented, mechanically ventilated, and MAC was determined using a tail-clamp method. Next, spontaneous ventilation was re-established, and anesthetic concentration was increased to determine the AC. Throughout the anesthetic event, heart rate (HR), systolic blood pressure (SAP), mean blood pressure (MAP), diastolic blood pressure (DAP), respiratory rate (RR), end-tidal carbon dioxide (Pe′CO2), and oxyhemoglobin saturation (SpO2) were recorded at 3-minute intervals. Following AC determination, AI was calculated as AC/MAC, and dogs were allowed to recover. Each dog was anesthetized four times (twice with ISO and SEVO each) at 1-week intervals. All data were analyzed using the two-way anova. Multiple comparisons were performed between ISO and SEVO treatments. Statistical significance was set at p < 0.05. Significant differences were noted between agents for MAC (SEVO, 2.13 ± 0.10%; ISO, 1.38 ± 0.14%; p < 0.0001), AC (SEVO, 7.34 ± 0.13%; ISO, 3.60 ± 0.13%; p < 0.0001), and AI (SEVO, 3.46 ± 0.22; ISO, 2.63 ± 0.14; p = 0.0002). Physiologic parameters were compared between SEVO and ISO at 1MAC, 2MAC, 3MAC, and AC. No differences were noted between SEVO and ISO treatments for cardiovascular parameters (HR, SAP, MAP, DAP). Significant differences were noted, favoring SEVO, for all respiratory parameters (RR, Pe′CO2, SpO2) at increasing MAC multiples. Additionally, regression analysis was conducted for physiologic variable data points. Analysis of Pe′CO2 data points demonstrated a significant slope difference of −6.47 ± 1.02 (BSEVO − BISO; p < 0.0001; r2 = 0.6042) favoring SEVO. While expected dose-related ventilatory depression was noted for both agents, all the respiratory parameters for SEVO demonstrated less respiratory depression than ISO at equipotent doses. These results indicated that SEVO caused less dose-dependent ventilatory depression than ISO, having a significantly higher AI and causing less detrimental change in pulmonary parameters at increasing levels of MAC.

Pharmacokinetics of propofol as an induction agent in geriatric dogs

The pharmacokinetics of propofol were investigated in six unpremedicated dogs aged between eight-and-a-half and 10·5 years. After the induction of anaesthesia with a bolus dose of 5 mg kg −1 propofol administered intravenoously, the trachea was intubated and anaesthesia was maintained with halothane in a gas mixture of oxygen and nitrous oxide. The mean (sd) t 1 2 β was 83·9 (14·8) minutes, the mean (SD) residence time was 99·0 (10·8) minutes, the mean body clearance was 34·5 (12·1) ml kg −1 minute 1 and the mean volume of distribution at steady state was 3864 (1647) ml kg-1. The dose of propofol was lower than that recommended in the data sheet (6·5 mg kg −1) and was associated in some of these dogs over eight years of age with post-induction apnoea. The clearance of propofol was also slower than that previously reported in young dogs. These results have implications for infusion rates when propofol is used to maintain anaesthesia in dogs

Effects of medetomidine premedication on propofol infusion anaesthesia in dogs

Observations of cardiovascular and respiratory parameters were made on six dogs anaesthetized on two separate occasions for 120 minutes with a propofol infusion, once without premedication and once following premedication with 10 μg kg −1 of intramuscular medetomidine. During anaesthesia the heart rate and cardiac index tended to be lower following medetomidine premedication, while the mean arterial pressure was significantly greater (p<0.05). Although the differences were not statistically significant, the systemic vascular resistance, pulmonary vascular resistance and stroke volume index were also greater in dogs given medetomidine. The mean arterial oxygen and carbon dioxide tensions were similar under both regimens, but in 2 dogs supplementary oxygen had to be administered during anaesthesia to alleviate severe hypoxaemia on both occasions they were anaesthetized. Minute and tidal volumes of respiration tended to be greater in dogs not given medetomidine but medetomidine premedication appeared to have no effect on venous admixture. Dogs given medetomidine received intramuscular atipamezole at the end of the 120 min. propofol infusion; the mean time from induction of anaesthesia to walking without ataxia was 174. min in the unpremedicated dogs and 160 min. in the dogs given atipamezole. The mean blood propofol concentration at which the dogs walked without ataxia was higher in the unpremedicated animals (2.12 ± 0.077 μg. ml −1 compared with 1.27 ± 0.518 μg. ml −1 in the premedicated dogs). The oxygen delivery to the tissues was lower after medetomidine premedication (p = 0.03) and the oxygen consumption was generally lower after medetomidine premedication but the difference did not achieve statistical significance. No correlation could be demonstrated between blood propofol concentration and cardiac index, systemic or pulmonary vascular resistance indices, systolic, diastolic or mean arterial blood pressures.

Median effective dosage of propofol for induction of anesthesia in dogs

Summary The median effective dosage (ed50) of propofol for induction of anesthesia was determined in 25 dogs premedicated with acepromazine, 0.05 mg/kg of body weight, and in 35 unpremedicated dogs. The ed50 was found to be 2.2 mg/kg in premedicated dogs and was 3.8 mg/kg in unpremedicated dogs. The mean ± sd total dosage of propofol required to induce anesthesia in premedicated animals was 2.8 ± 0.5 mg/kg and was 4.7 ± 1.3 mg/kg in unpremedicated animals. Signs of excitement were observed in 5 of the unpremedicated dogs, but in none of those that were premedicated.

Clinical evaluation of propofol as an intravenous anaesthetic agent in cats and dogs

The clinical efficacy and safety of an emulsion containing 10 mg/ml of the intravenous anaesthetic propofol were evaluated in cats and dogs by veterinary surgeons in eight practices in the United Kingdom. A total of 290 dogs and 207 cats were anaesthetised with propofol either as a single injection for procedures of short duration, or as an induction agent with maintenance provided by further incremental injections or as an induction agent with maintenance by gaseous agents. The mean induction doses of propofol for unpremedicated dogs and cats were respectively 6.55 mg/kg and 8.03 mg/kg. The mean induction doses after premedication with a tranquilliser were 4.5 mg/kg and 5.97 mg/kg for dogs and cats, respectively. Mean recovery times ranged, depending on the method of anaesthesia, from 23 to 40 minutes in dogs and from 27 to 38 minutes in cats; recovery was defined as the time at which the animals were alert and able to stand. Adverse side effects were infrequent, apnoea during induction being the commonest. Acepromazine and atropine were most often used as premedicants although in a few cases diazepam, xylazine and other agents were employed. No clinical incompatibility was observed between propofol and any of the other agents administered during the study. The rapid and usually excitement-free recovery of the animals was a valuable feature of anaesthesia with propofol.

Propofol as an intravenous anaesthetic agent in dogs.

Studies in dogs with an emulsion formulation of the intravenous anaesthetic, propofol, showed that induction of anaesthesia was smooth and it was possible to maintain anaesthesia by intermittent injection. The mean dose for induction of anaesthesia in unpremedicated dogs was 5.95 mg/kg body-weight. When no premedication was administered anaesthesia was maintained by a total dose of approximately 0.806 mg/kg/minute. Premedication with between 0.02 and 0.04 mg/kg of acepromazine reduced the mean induction dose by about 30 per cent and the maintenance dose by more than 50 per cent. In 68 unpremedicated dogs given one dose, recovery was complete in a mean time of 18 minutes and after maintenance of anaesthesia by intermittent injection in 65 dogs the mean recovery time was 22 minutes from administration of the last dose. Premedication with acepromazine did not produce statistically significant increases in these recovery times. The quiet, rapid and complete recovery proved to be most valuable in cases where the animal had to be returned to the owners' care with the minimum of delay.

R 8110, a new short-acting hypnotic in dogs

The clinical, respiratory and cardiovascular effects of intravenous injections of R 8110, a fluor analogue of etomidate, were studied in unpremedicated dogs. Clinical observations were carried out after intravenous injections of 3 and 4 mg kg-1 of R 8110. Cardiovascular studies were conducted after an intravenous injection of 3 mg kg-1. The drug proved to be a safe and reliable agent for induction and produced a short-lasting hypnosis and some analgesia. Both induction and recovery were smooth and rapid. Heart rate and systolic and diastolic blood pressure decreased significantly (P less than or equal to 0.05) 10 minutes after injection; the influence on arterial blood parameters was minimal.

Epinephrine arrhythmogenicity is enhanced by acute, but not chronic, aminophylline administration during halothane anesthesia in dogs.

The authors determined the effect of acute and chronic aminophylline treatment on the arrhythmogenicity of epinephrine during halothane anesthesia. The dose of epinephrine required to achieve an arrhythmia threshold (ADE) was determined in nine unpremedicated dogs anesthetized with halothane (1.5% v/v) in oxygen (A0). Aminophylline was then infused to achieve and sustain a therapeutic theophylline level (mean +/- SD) of 17 +/- 2 micrograms X ml-1 (A1), at which time the ADE was reassessed. The aminophylline infusion regimen was then adjusted to provide a supratherapeutic level of theophylline of 34 micrograms X ml-1 (A2) and the ADE was reassessed. In an additional seven dogs the ADE was assessed before and after 6 weeks of oral aminophylline treatment that yielded a plasma theophylline level of 18 +/- 3 micrograms X ml-1. The ADE was significantly (P less than 0.01) reduced from a basal value (mean +/- SD) of 2.63 +/- 0.97 micrograms X kg X -1 X min-1 to 1.39 +/- 0.47 in the A1 state. There was no further decrement in the ADE at the A2 state (1.17 +/- 0.36). The plasma epinephrine level at the arrhythmia threshold decreased commensurately from 50.7 +/- 40.2 ng X ml-1 (A0) to 20.0 +/- 7.9 and 19.2 +/- 7.6 in the A1 and A2 states, respectively (P less than 0.01). In contrast to these acute treatment experiments, neither the ADE (2.65 +/- 0.95 vs. 2.97 +/- 1.49 micrograms X kg-1 X min-1) nor the plasma epinephrine levels at the arrhythmia threshold (47.2 +/- 13.7 vs. 51.1 +/- 22.0 ng X ml-1) were different after chronic aminophylline treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

The relationship of age to canine cerebral metabolic rate

In 15 unpremedicated dogs, an inverse relationship between age and cerebral metabolic rate (CMR O 2 ) was observed. In dogs estimated to be 0.5 to 1.5 and 1.5 to 3 years of age, the mean CMR O 2 values (5.27 and 4.85 ml./100 gm./min.) were significantly greater than that value of dogs more than 3 years old (4.22 ml./100 gm./min.). No difference in metabolic pathways between the groups was observed. The relative magnitude of the effect of age on CMR O 2 is similar to that reported for man (assuming a 1:7-year ratio). Such an effect provides a significant potential source of error when comparing individual cerebral metabolic studies in animals of a different or an unknown age.

The effect of nitrous oxide on canine cerebral metabolism.

Cerebral blood flow and arterial–sagittal differences for oxygen have been measured in unpremedicated dogs maintained at, 37.0 C. All were paralyzed, had received a spinal anesthetic, and were artificially ventilated. In each of a first group, measurements with and without halothane were carried out with 70 per cent N2O in O2 and with 70 per cent N2 in O2. In a second group, either N2O or N2 was used throughout and measurements were made in the absence of halothane and at 0.1, 0.4, and 0.7 per cent halothane (alveolar). In the absence of halothane and at 0.1 per cent halothane, the average rate of consumption of O2 by the brain (CMRo2) was 11 per cent greater with N2O than with N2. At 0.4 and 0.7 per cent halothane, CMRo2 was greater with N2O but the differences were not significant. It is concluded that N2O per se is not a cerebral metabolic depressant and that the anesthetic action of N2O is not based on generalized cerebral metabolic depression.

The effect of halothane on canine cerebral metabolism.

Cerebral blood flow (CBF) and arterial-sagittal sinus differences for oxygen, glucose, and lactate have been measured in ten unpremedicated dogs maintained at 37.0° C and ventilated with 0 to 2 per cent halothane in N2O (70 per cent) and O2. Flows were determined by a direct method which collects the venous drainage of portions of both cerebral hemispheres. With halothane, the rate of consumption of O2 by the brain (CMRo2) was reduced 17 per cent (mean) while CBF and sagittal sinus Po2 increased. Oxygen/glucose and lactate/glucose indices were unchanged. Since the reduction in CMRo2 with halothane was apparently neither based on an impaired oxygen supply nor associated with alteration of cerebral metabolic pathways, it is concluded that halothane is a direct cerebral metabolic depressant.

Methoxyflurane: Effects upon cardiac contractility, rhythmicity, and blood pressure in dogs

Methoxyflurane was administered to unpremedicated dogs in increasing and decreasing cpncentrations while normal pulmonary ventilation was rigidly maintained. Myocardial contractility, blood pressure, pulse rate, electrocardiogram, and electroencephalogram were recorded continuously. A progressive decrease in contractile force of the heart muscle resulted as the inhaled concentration of methoxyflurane increased. A parallel decrease in systolic, diastolic, and pulse pressure occurred. Sinus bradycardia and an alteration in repolarization of cardiac muscle accompanied the dynamic changes. A lag occurred in recovery of all cardiovascular functions and the EEG following withdrawal of the agent. Burst suppression appeared when hypotension below 90 mm. Hg occurred. A comparison of the results of this study with those previously reported is presented.